Published online before print June 13, 2005, doi: 10.1161/01.HYP.0000171478.40560.3c
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(Hypertension. 2005;46:29.)
© 2005 American Heart Association, Inc.
Editorial Commentaries |
Aldosterone Promotes Endothelial Dysfunction Via Prostacyclin Independent of Hypertension
From the Tulane Hypertension and Renal Center of Excellence (F.K.J., R.A.J.), and Department of Physiology, Tulane University Health Sciences Center, New Orleans, La; and the Michael E. DeBakey VA Medical Center (W.D.), and Departments of Medicine and Pharmacology, Baylor College of Medicine, Houston, Tex.
Correspondence to Fruzsina K. Johnson, MD, Assistant Professor, Department of Physiology, Tulane University Health Sciences Center, 1430 Tulane Avenue, SL-39, New Orleans, LA 70112. E-mail Fruzsi123@aol.com
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The renin-angiotensin-aldosterone system plays a key role in the regulation of blood pressure and water/electrolyte homeostasis. Classically, angiotensin II causes arteriolar vasoconstriction and increases aldosterone levels, whereas aldosterone promotes sodium and water reabsorption and potassium secretion via renal mineralocorticoid receptors. It is now well-accepted that inappropriate activation of the renin-angiotensin-aldosterone system not only increases blood pressure but also can play an important role in end-organ damage. Although Selye et al have demonstrated that administration of a mineralocorticoid combined with sodium promotes malignant hypertension and end-organ damage,1 subsequent clinical and experimental studies have focused on the pathological effects of angiotensin II, rather than aldosterone, and demonstrated that angiotensin-converting enzyme inhibitors, as well as angiotensin II receptor antagonists, confer significant cardiovascular protection.
Recent discoveries have revolutionized our view of aldosterone and its biological actions, and identified mineralocorticoids as important mediators of cardiovascular injury.2,3 The demonstration of rapid aldosterone effects challenged the exclusive role of mineralocorticoid receptor-mediated genomic actions in aldosterone signaling.4 Furthermore, it is now well-established that aldosterone can exert effects in nonepithelial and extrarenal tissues.2 Moreover, mineralocorticoids not only exert effects on extrarenal tissues but also can be synthesized outside the adrenal cortex.5 Aldosterone has now been shown to promote cardiovascular inflammation, endothelial dysfunction, and fibrosis.2 Furthermore, the effects of aldosterone can be independent of blood pressure, because mineralocorticoid receptor blockade can confer cardiovascular protection without lowering the blood pressure.6 In the light of these advancements, recent clinical trials have shown the cardiovascular protective benefits of mineralocorticoid receptor blockade.7
In this
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Hypertension 2005 46: 107-112.
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